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Aminoacyl‐tRNA synthetase gene regulation in Bacillus subtilis : induction, repression and growth‐rate regulation
Author(s) -
Putzer Harald,
Laalami Soumaya,
Brakhage Axel A.,
Condon Ciarán,
GrunbergManago Marianne
Publication year - 1995
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1995.tb02432.x
Subject(s) - antitermination , biology , transfer rna , bacillus subtilis , psychological repression , derepression , overproduction , gene , stringent response , transcription (linguistics) , effector , terminator (solar) , regulation of gene expression , genetics , microbiology and biotechnology , biochemistry , gene expression , rna , rna polymerase , bacteria , escherichia coli , astronomy , ionosphere , linguistics , philosophy , physics
Summary The thrS gene in Bacillus subtilis is specifically induced by starvation for threonine and is, in addition, autorepressed by the overproduction of its own gene product, the threonyl‐tRNA synthetase. Both methods of regulation employ an antitermination mechanism at a factor‐independent transcription terminator that occurs just upstream of the start codon. The effector of the induction mechanism is thought to be the uncharged tRNA Thr , which has been proposed to base pair in two places with the leader mRNA to induce antitermination. Here we show that the autoregulation by synthetase overproduction is likely to utilize a mechanism similar to that characterized for induction by amino acid starvation, that is by altering the levels of tRNA charging in the cell. We also demonstrate that the base pairing interaction at the two proposed contact points between the tRNA and the leader are necessary but not always sufficient for either form of regulation. Finally, we present evidence that the thrS gene is expressed in direct proportion to the growth rate. This method of regulation is also at the level of antitermination but is independent of the interaction of the tRNA with the leader region.

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